Mediterranean Diet and Its Association with Cardiovascular Disease Risk Factors: A Scoping Review
Abstract
:1. Introduction
2. Materials and Methods
3. Results
3.1. Clinical Trials
3.2. Genetics
3.3. Biomarkers for Stress and Inflammation
3.4. Blood Pressure, Lipids, and Anthropometric Measurements
3.5. Carotid Intima-Media Thickness, Flow-Mediated Dilation, and Plaque Height
3.6. MedDiet Adherence
3.7. Observational Studies
3.8. Biomarkers for Stress and Inflammation
3.9. Insulin Measures, Lipids, and Lipoproteins
3.10. Plaque and Arterial Health
3.11. Subclinical Atherosclerosis Measurements
3.12. Scoring Measures of Heart and Vascular Health
3.13. MedDiet Adherence
4. Discussion
4.1. Clinical Studies
4.2. Observational Studies
4.3. Strengths and Limitations
4.4. Future Directions
5. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Conflicts of Interest
References
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Food Group | Bioactive Compounds | Association with CVD Risk Factors |
---|---|---|
Fruits | Polyphenols 3 Fiber 2 Ascorbic acid 6 Vitamin C 6 Myricetin 6 Quercetin 6 Anthocyanins 6 Cyanidins 6 Flavonols 6 Ascorbic Acid 6 | Decrease CVD 1 Decrease cholesterol 6 Inhibit LDL-C oxidation 6 Decrease Blood Pressure 6 |
Vegetables | Polyphenols 3 Fiber 2 Carotenoids 6 Vitamin C 6 Lycopene 6 | Decrease CVD 1 Decrease Blood Pressure 3 Decrease cholesterol 6 Inhibit LDL-C oxidation 6 |
Whole Grains | Phytochemicals 6 Fiber 3 K+, Mg2+, and Ca2+ 3 | Decrease Cholesterol 3 Increase Glycemic Control 3 Reduce T2DM Risk 3 Decrease Blood Pressure 3 Decrease Adiposity 3 |
Nuts | Fiber 3 K+, Mg2+, and Ca2+ 3 Phytosterols 6 Linolenic acids 2 Tocopherols 6 Omega-3s 6 | Decrease Cholesterol 3 Decrease Triglycerides 3 Decrease Blood Pressure 3 Reduce T2DM Risk 3 |
Legumes | Polyphenols 6 Fiber 3 K+, Mg2+, and Ca2+ 3 | Decrease CVD 1 Decrease Blood Pressure 3 Decrease cholesterol 6 |
Olive Oil | Polyphenols 3 Phytosterols 3 MUFA 3 | Decrease CVD 1 Decrease Adiposity 3 Decrease Blood Pressure 3 Inhibit LDL-C oxidation 6 Decrease Inflammation 3 Reduce T2DM Risk 3 |
Fish | Omega-3s 6 | Decrease Triglycerides 3 Increase HDL 3 Decrease cholesterol 6 Inhibit LDL-C oxidation 6 Decrease Blood Pressure 6 |
Red Wine (Moderate) | Polyphenols 3 Resveratrol 2 Myricetin 6 Quercetin 6 Anthocyanins 6 Cyanidins 6 Flavonols 6 | Decrease Adiposity 3 Decrease Blood Pressure 3 Decrease Inflammation 3 Reduce T2DM Risk 3 |
Meat and meat products § | L-carnitine 7 L-carnosine 7 Choline 7 Lipoic acid 7 Conjugated dienes of linoleic acid (CLA) 7 Glutathione 7 Taurine 7 Coenzyme Q10 7 Creatine 7 | Decrease Blood Pressure 7 Decrease Inflammation 7 Reduction of Fat Mass 7 |
Dairy | Calcium 5 Conjugated linoleic acid 5 Glycomacropeptide 5 Lactoferrin 5 β–Lactoglobulin 5 | Decrease Blood Pressure 4 Decrease Inflammation 4 Reduce T2DM Risk 4 |
Author/Year [Location] | Study Design/Length | Intervention | Participants/Major Cohort | Comparison Group | Diabetes: Y/N | Clinical Measurements | Outcome Associated w/Higher MedDiet Adherence |
---|---|---|---|---|---|---|---|
Medina-Remon et al. (2017) [Spain] [17] | RCT, 1y | MD-EVOO, MD-Nuts, LFD | High CVD Risk, 55–80 yo men & 60–80 yo women (n = 1139)/PREDIMED | Baseline Comparison | Y | Urine Total Polyphenols (UTP), SBP, DBP, Fasting Glucose, TC, LDL-C, HDL-C, TG, VCAM-1, ICAM-1, IL-6, TNF-α, MCP-1 | UTP T1: ↓UTP, ⦸SBP, ⦸DBP, ⦸Fasting Glucose, ⦸TC, ↓LDL-C, ↑HDL-C, ⦸TG, ⦸VCAM-1, ⦸ICAM-1, ⦸IL-6, ⦸TNF-α, ⦸MCP-1 UTP T2: ↑UTP, ↓SBP, ↓DBP, ⦸Fasting Glucose, ⦸TC, ↓LDL-C, ↑HDL-C, ⦸TG, ⦸VCAM-1, ⦸ICAM-1, ↓IL-6, ↓TNF-α, ⦸MCP-1 UTP T3: ↑UTP, ↓SBP, ↓DBP, ⦸Fasting Glucose, ⦸TC, ↓LDL-C, ↑HDL-C, ⦸TG, ↓VCAM-1, ↓ICAM-1, ↓IL-6, ↓TNF-α, ↓MCP-1 |
Torres-Pena et al. (2018) [Cordoba, Spain] [18] | RCT, 1.5y | MedDiet v. LFD | CHD Patients w/no events in the last 6 months, 20–75 yo, life expectancy of at least 5 years, prediabetes (n = 289), T2D (n = 438), and no T2D (n = 78) (n = 805)/CORDIOPREV | LFD (n = 387) | Y | FMD | ↑FMD in MedDiet + Prediabetes and MedDiet + Diabetes (Baseline to 1.5y) MedDiet v. LFD in patients with Diabetes: ↑FMD MedDiet & LFD in patients w/o Diabetes: ⦸ FMD |
Casas et al. (2018) [Barcelona, Spain] [30] | RCT, 5y | MD-EVOO, MD-Nuts, LFD | High CVD Risk, 55–80 yo men & 60–80 yo women (n = 160)/PREDIMED | LFD (n = 52) | Y | CVD Risk factors: SBP, DBP, TGs, Total-C, HDL-C, LDL-C, Total:HDL-C, Glucose, Glycated hemoglobin, Wt, BMI, WC T-lymphocytes: CD11a, CD49d, & CD40 Monocytes: CD11a, CD11b, CD49d, & CD40 Circulating Markers: MCP-1, IL-6, TNF-α, & hs-CRP | CVD Risk Factors: Baseline v. 5y: ↓SBP, DBP, LDL-C, Total-C, Total:HDL-C, TG, Wt, BMI, & WC; ↑HDL-C; ⦸Glucose, Glycated Hemoglobin, 5y: MD v. LFD: ↓SBP, DBP, LDL-C, Wt, & BMI ⦸ TG, Total-C, HDL-C, Total-HDL-C, Glucose, Glycated Hemoglobin, & WC T-Lymphocytes: Baseline v. 5y: ↓CD11a, CD49d, & CD40 5y MD v. LFD: ↓CD11a, CD49d, & CD40 Monocytes: Baseline v. 5y: ↓CD11a, CD11b, CD49d, & CD40 5y MD v. LFD: ↓CD11a, CD11b, CD49d, & CD40 Circulating Markers: Baseline v. 5y: ↓MCP-1, IL-6, TNF-α, & hs-CRP 5y MD v. LFD: ↓MCP-1, IL-6, TNF-α, & hs-CRP |
Camargo et al. (2012) [Spain] [51] | RCT-Crossover, 9w | MD-VOO, SFA-Rich, CHO-PUFA | Healthy, elderly (n = 20) | SFA-Rich and CHO-PUFA | N | Inflammation Genes: NF-kB (p65 & IkBα), MCP-1, TNF-α, IL-6 Plaque Stability Gene: MMP-9 & MIF-1 | Compared to SFA-Rich: Fasting: ↓p65, ⦸NF-kB (IkBα), MCP-1, TNF-α, IL-6, MIF-1, MMP-9 Postprandial: ↓p65, MCP-1, MMP-9 ↑IkBα, ⦸TNF-α, IL-6, Compared to CHO-PUFA-Rich: Fasting: ⦸ All measures Postprandial: ↓p65 & TNF-α, ↑IkBα, ⦸MCP-1, IL-6, MMP-9, & MIF-1 |
Di Renzo et al. (2018) [Rome, Italy] [52] | RCT, 2h | Only: (a) Red Wine (RW), (b) White Wine (WW), (c) Vodka (V); Only: (d) MedDiet or (e) a High-Fat Meal (HFM); Combination: (f)MedDiet + RW (g) MedDiet + WW (h) MedDiet + V (i) HFM + RW (j) HFM + WW (k) HFM + V | 18–65 yo, BMI between 18.5–35 kg/m2, otherwise healthy adults (n = 55) | Baseline Comparison | N | oxLDL-C Gene expression: Catalase (CAT), superoxide dismutase 2 (SOD2), and glutathione peroxidase 1 (GPX1) | Baseline to post-intervention: ↑ oxLDL-C (HFM-only), ⦸ All other beverages, ⦸ All diet, and ⦸All combinations; Among treatments: MedDiet v. HFM: ↓oxLDL-C (MedDiet), ↑oxLDL-C (HFM), MedDiet + RW v. HFM: ↓oxLDL-C (MedDiet + RW), ↑oxLDL-C (HFM) CAT Regulation: ↑RW, ↓WW, V, HFM + WW, & HFM+V SOD2 Regulation: ↑ WW, MedDiet + V, and RW ↓HFM+V GPX1 Regulation: ↑RW, MedDiet+RW, and HFM+RW |
Storniolo et al. (2017) [Reus and Barcelona, Spain] [53] | RCT, 1y | MD-EVOO, MD-Nuts, LFD | Non-smoker, hypertensive women, 60–80 yo, not consuming non-steroidal anti-inflammatory drugs w/o CVD, but at high risk of CVD (n = 90)/PREDIMED | LFD (n = 30) | Y | BP, serum nitric oxide (NO) and endothelin-1 (ET-1) Antioxidant capacities: total antioxidant capacity (TAC), malondialdehyde (MDA) Gene expression: endothelial NO synthase (eNOS), caveolin 2 (CAV2) and endothelin-1 receptors (ETAR and ETBR) | MD-Nuts: ↓DBP, serum ET-1 MD-EVOO: ↑NO; ⦸ antioxidant capacity and MDA Change in Gene Expression: MD-Nuts: ↓eNOS, CAV2, ET-1 receptors (A and B); MD-EVOO: ↓CAV2 and ET-Receptor B |
Urpi-Sarda et al. (2021) [Barcelona and Valencia, Spain] [54] | RCT, 3y | MD-EVOO, MD-Nuts, LFD | High CVD Risk, 55–80 yo men & 60–80 yo women (n = 285)/PREDIMED | LFD (n = 100) | Y | Plasma Markers: CRP, IL-1β, IL-6, IL-8, IL-12p70, IL-18, TNF-α, MCP-1, RANTES/CCL5, MIP-1β/CCL4, IP-10/CXCL10, ENA78/CXCL5, I-TAC/CXCL11 & IFN-γ Genes: TLR2, TLR4, TLR6, NLRP3, CASP-1, IL1R1, CCR2, CCR5, CXCR2, CXCR3 | ↓ CRP, IL-1β, IL-6, IL-8, IL-12p70, TNF-α, MCP-1, RANTES/CCL5, MIP-1β/CCL4, ENA78/CXCL5, & IFN-γ ⦸ IP-10, I-TAC, & IL-18 ⦸ All Genes |
Casas et al. (2016) [Barcelona, Spain] [55] | RCT, 1y | MD-EVOO, MD-Nuts, LFD | High CVD Risk, 55–80 yo men & 60–80 yo women (n = 164)/PREDIMED | LFD (n = 54) | Y | CVD Risk factors: SBP, DBP, TGs, Total-C, HDL-C, LDL-C, Total:HDL-C, Glucose, Glycated hemoglobin, Wt, BMI, WCT-lymphocytes: CD11a, CD49d, CD40 Monocytes: CD11a, CD11b, CD49d, & CD40 Circulating Markers: sVCAM, sICAM, sE-SEL, sP-SEL, IL-6, CRP, IL-18, IL-10, IL-18/IL-10 Ratio, MMP-9, TIMP-1, MMP-9/TIMP-1 ratio, TGF-β1 | CVD Risk Factors: Baseline v. 1y: ↓WC, SBP, DBP, Total-C, LDL-C, & Total:HDL-C; ⦸WT, BMI, Glucose, Glycated Hemoglobin, TG, HDL-C MD v. LFD: ↓SBP, DBP, Total-C, LDL-C, Total:HDL-C; ⦸Wt, BMI, WC, Glucose, Glycated Hemoglobin, TG, & HDL-C T-Lymphocytes: Baseline v. 1y:↓ CD11a, CD49d, CD40 MD v. LFD: ⦸CD11a, CD49d, CD40 Monocytes: Baseline v. 1y: ↓CD40, CD11a, CD11b, & CD49d MD v. LFD: ↓CD40 ⦸CD11a, CD11b, & CD49d Circulating Markers: Baseline v. 1y:↓sVCAM, sICAM, sE-SEL, sP-SEL, IL-6, CRP, IL-18, IL-18/IL-10 ratio; ↑ TGF-β1; ⦸ IL-10, MMP-9, TIMP-1, MMP-9/TIMP-1 ratio MD v. LFD: ↓sP-SEL, IL-6, CRP, IL-18/IL-10 Ratio |
Castaner et al., 2013 [Spain] [56] | RCT, 3m | MD-EVOO, MD-Nuts, LFD | men aged 55–80 y, women aged 60–80 y with at least one of the following criteria: (1) T2D or (2) 3 or more CVD risk factors [current smoking, hypertension (BP > 140/90 mm Hg or treatment with antihypertensive drugs), LDL-C concentration > 160 mg/dL (or treatment with hypolipidemic drugs), HDL-Cconcentration < 40 mg/dL, BMI (in kg/m2) > 25, or a family history of premature CAD (n = 34)/PREDIMED | LFD (n = 12) | Y | BMI, WC, SBP, DBP, Glucose, TC, LDL-C, HDL-C, TG, ApoA-I, Apo B-100, OxLDL, CRP, Hydroxytyrosol, IL1β, IL1RN, TNF-α, ICAM1, VEGF Signaling Pathways: Role of NFAT in Cardiac Hypertrophy, P2 gamma Purigenic Receptor Signaling Pathway, Hypoxia Signaling in the CVD, Cardiac Hypertrophy Signaling, Renin-Angiotensin Signaling, Inhibition of Angiogenesis by TSP1, Angiopoietin Signaling, Nitric Oxide Signaling in the CVS, Atherosclerosis Signaling, eNOS Signaling, Factors Promoting Cardiogenesis in Vertebrates, Aldostrone Signaling in Epithelial Cells, Cardiac Beta-adrenergic Signaling, HIF1alpha Signaling, Cardiomyocyte Differentiation via BMP Receptors, Thrombin Signaling, Endothelin-1 signaling, and Cellular Effects of Sildenafil | ↓BMI (MD-Nuts & MD-EVOO), ↓WC (MD-Nuts), ↓SBP (MD-VOO), ⦸DBP, ⦸Glucose, ⦸TC, ⦸LDL-C, ⦸HDL-C, TG, ⦸ApoA-I, ⦸Apo B-100, ⦸OxLDL, ⦸CRP, ⦸Hydroxytyrosol Signaling Pathways: (MD-EVOO + MD-Nuts):↓Hypoxia Signaling in the CVS, ↓eNOS Signaling, ↓Nitric Oxide Signaling in the CVS, ↓Renin-Angiotensin Signaling, ↓Aldosterone Signaling in Epithelial Cells, ↓P2 gamma Purigenic Receptor Signaling Pathway, ↓Cardiac Hypertrophy Signaling MD-EVOO (only): ↓Atherosclerosis, ↓Nitric Oxide Signaling in the CVS, ↓Angiopoietin Signaling, ↓Renin-Angiotensin Signaling, ↓Role of NFAT in Cardiac Hypertrophy, and ↓Cardiac Hypertrophy Signaling |
Duś-Zuchowska et al. (2018) [57] [Poland] | RCT, 16w | MedDiet v. Central European Diet (CED) | Obese, postmenopausal women, nonsmokers with a risk of Metabolic Syndrome (MS) (n = 144) | Baseline Comparison | N | hs-CRP and asymmetrical dimethylarginine (ADMA) | Within group comparisons: ↓hs-CRP Between Group Comparison: ⦸hs-CRP Within group comparisons: ↓ADMA (CED-only) Between Group Comparison: ⦸ADMA |
Marin et al. (2011) [58] [Spain] | RCT, Crossover, 4w | saturated fatty acid (SFA) diet; a LFHC diet; and a MedDiet | Free living, elderly (>65 yo), free of chronic illness (hepatic, renal, thyroid, or cardiac dysfunction) (n = 20) | Cross comparison | Y | TC, TG, HDL-C, LDL-C, ApoA-I, ApoB, ischemic reactive hyperemia (IRH), Superoxide dismutase activity, β-Carotene, Catalase activity, Isoprostane, Lipoperoxides, ⍺-Tocopherol, OxLDL, Nitric Oxide, Protein Carbonyl activity, Nitrotyrosine, Glutathione peroxidase activity Total MPs, Apoptotic EMPs, Activated EMPs, %EPCs | ↓TC, LDL-C, ApoB, Superoxide dismutase activity, Isoprostane, Lipoperoxides, and Nitrotyrosine ↑IRH, β-Carotene ⦸ TG, HDL-C, ApoA-I, Catalase Activity, ⍺-Tocopherol, OxLDL, Nitric Oxide, Protein Carbonyl activity ↓ Total MPs, Apoptotic EMPs, Activated EMPs, ↑ %EPCs |
Yubero-Serrano et al. (2020) [Cordoba, Spain] [59] | RCT, 1y | MedDiet v. LFD | CHD Patients w. no events in the last 6 months, 20–75 yo, life expectancy of at least 5 years (n = 805)/CORDIOPREV | LFD (n = 387) | Y | Flow-Mediated Dilation (FMD), endothelial microparticles (EMPs), and endothelial progenitor cells (EPCs) | When FMD <2% and FMD>2%: MedDiet v. LFD: ↑FMD, ↓EMP (Activated & Apoptotic), and ↑EPC MedDiet v. LFD: ⦸BMI, ⦸LDL-C, ↑HDL-C, ⦸TC, ⦸TG, ↓Fasting Glucose, ⦸Fasting Insulin, ⦸HbA1c, ↓hsCRP ↓EMPs, ROS, cellular apoptosis, senescence ↑ cellular proliferation and angiogenesis |
Maiorino et al. (2016) [Naples, Italy] [60] | RCT, 8.1y | MedDiet v. LFD | Men and women with newly diagnosed T2D, overweight, never treated with antihyperglycemic drugs, HbA1c levels <11% (n = 215)/MEDITA | LFD (n = 107) | Y | endothelial progenitor cells (EPCs) and cIMTWeight, WC, HbA1c, Plasma Glucose, HOMA of insulin sensitivity, TC, HDL-C, Non-HDL-C, SBP, DBP, cIMT, CRP | MedDiet (Baseline, Year 2, Year 4, EOT) and compared to LFD(starting at Year 2): ↑CD34+KDR+, ↑CD34+KDR+CD133+ MedDiet: ↓cIMT; LFD: ⦸cIMT MedDiet (v. LFD): ↓Weight, WC, HbA1c, HOMA-IS, TC, SBP, ↑HDL-C |
Carnevale et al. (2014) [Italy] [61] | RCT, Crossover, 4w | Study 1: MedDiet w/EVOO and MedDiet w/o EVOO Study 2: MedDiet w/EVOO and MedDiet w/Corn Oil | Healthy adults working in research institute (n = 25) | Cross comparison | N | Platelet reactive oxidant species (ROS) and 8-iso-PGF2a-III, activity of NOX2, the catalytic sub-unit of NADPH oxidase, as assessed in platelets and serum, serum vitamin E and endothelial dysfunction | Study 1: MedDiet w/o EVOO: ↑platelet ROS, 8-iso-PGF2a-III, NOX2 activity, sE-selectin, sVCAM1 and ↓serum vitamin E; ⦸ in all measures for MedDiet + EVOO Study 2: Corn Oil: ↑platelet ROS, 8-iso-PGF2a-III, NOX2 activity, sE-selectin, sVCAM1 and ↓serum vitamin E; ⦸ in all measures for MedDiet + EVOO |
Gudban et al. (2021) [Israel] [62] | RCT, 3m | MedDiet Intervention v. No intervention | T2D patients, 18yo+, adults, otherwise healthy (no other chronic diseases or conditions) (n = 22) | No intervention (n = 10) | Y | BMI, FMD%, CRP, ICAM-1, TC, TG, and HbA1c | ⦸ BMI, HbA1c, TC, TG ↓ CRP, ICAM-1 ↑FMD% |
Murie-Fernandez et al. (2011) [Navarra, Spain] [63] | RCT, 1y | MD-EVOO, MD-Nuts, LFD | High CVD Risk, 55–80 yo men & 60–80 yo women (n = 187)/PREDIMED | LFD (n = 62) | Y | Carotid intima-media thickness (cIMT) | 1-year change: ↓cIMT in MD+Nuts, ⦸ MD+EVOO, ⦸LFDAdjusted 1 year change: ↓cIMT in MD+Nuts and ↓MD+EVOO, ⦸LFD Univariate & Multivariate analysis: When cIMT >= 0.9 mm, MD-EVOO + MD-Nuts: ↓cIMT, ⦸LFD; For Multivariate Analysis: When cIMT >= 0.9 mm, MD-EVOO ↓cIMT and MD-Nuts ↓cIMT, ⦸LFD When cIMT < 0.9 mm, ⦸All diets |
Sala-Vila et al. (2014) [Spain] [64] | RCT, 2.4y | MD-EVOO, MD-Nuts, LFD | High CVD Risk, 55–80 yo men & 60–80 yo women (n = 164)/PREDIMED | LFD (n = 61) | Y | plaque height and cIMT of three prespecified segments (ICA, bifurcation (BIF), and common (CCA)) | LFD: ↑ICA-IMT(Mean), ↑ plaque (max); MD-Nuts: ↓ICA-IMT (mean) ⦸ ICA-IMT (Max) and Plaque (Max); MD-EVOO: ⦸ICA-IMT (Mean), ICA-IMT (Max), and Plaque (MAX) ⦸ Between Group Differences: CCA-IMT (Max and Mean), BIF-IMT (Max and Mean) |
Authors, Year [Location] | Study Design/Length | Participants | Diabetes: Y/N | Clinical Measurements | Outcome Associated w/Higher MedDiet Adherence |
---|---|---|---|---|---|
Antoniazzi et al. (2021) [Brazil and Spain] [15] | Cross section | Confirmed Familial Hypercholesterolemia or LDL receptor variants, ≥20 yo (n = 190) | N | plasma LDL-C, apolipoprotein-B (ApoB), high sensitivity C-reactive protein (hs-CRP) | ⦸ LDL-C, ↓ApoB, ↓hs-CRP |
Buscemi et al. (2013) [Italy] [16] | Cross section | No DM, CHD, or Renal Failure, ≥18 yo (n = 929) | N | cIMT, HOMA-IR, Triglycerides (Tri)/HDL-C, asymptomatic carotid atherosclerosis (PC) | ⦸ cIMT, ↓HOMA-IR, ↓Tri/HDL-C, ⦸ asymptomatic carotid atherosclerosis (plaques and/or cIMT ≥ 0.9 mm) |
Barrea et al. (2019) [Italy] [65] | Cross section | Healthy, normal weight, 18–50 yo (n = 302) | N | TMAO | ↓TMAO |
Cesari et al. (2018) [Italy] [66] | Cross section | >90 yo, men and women in Mugello area, Tuscany, Italy (n = 421) | N | endothelial progenitor (EPCs) and circulating progenitor (CPCs) cells | 4th MedDiet Quartile v. Other Quartiles: ↑ EPCs (CD34+/KDR+, CD133+/KDR+, CD34+/CD133+/KDR+) ⦸ CPCs (CD34+, CD133+, CD34+/CD133+) |
Pignanelli et al. (2018) [Ontario, Canada] [67] | Prospective, 1y | Stroke, transient ischemic attack, and/or atherosclerotic patients (n = 276) | N | Total plaque area (TPA), trimethylamine N-oxide (TMAO), p-cresyl sulfate (PCS), hippuric acid (HA), indoxyl sulfate (IS), p-cresyl glucuronide (PCG), phenyl acetyl glutamine (PAG), & phenyl sulfate (PS) | ⦸ TPA, TMAO, PCS, HA, IS, PCG, PAG, & PS |
Shah et al. (2020) [USA] [68] | Cross section | Women enrolled in American Heart Association Go Red for Women Strategically Focused Research Network at Columbia University Irving Medical Center, BMI 25–33 kg/m2 or BMI 20–25 kg/m2 w/o immediate fam history of obesity, hypertension, or DM; absence of chronic diseases and chornic disease medication (n = 25) | N | NF- κB and eNOS | ⦸NF- κB and eNOS |
Witkowska & Zujko (2014) [Poland] [69] | Cross section | 19–22 yo, women, BMI ≤ 25 kg/m2, without inflammatory, autoimmune, or metabolic diseases (n = 25) | N | sICAM-1, sVCAM-1, and E-selectins | ⦸ VCAM-1 and ICAM-1 ↓sE-selectin |
Millar et al. (2021) [Ireland] [70] | Cross section | Clinical random sample, 46–73 yo, White European (n = 1862) | Y | Plasma Lipids: TotChol, TG, LDL-C, HDL-C Lipoprotein particle concentrations: TotTRL, S-, M-,&L-VLDL; S-, L- & T-LDL; S-, M-, L-, T-HDL; IDL Lipoprotein particle size: VLDL, LDL, HDL, LP-IR | ⦸ All Plasma Lipids ⦸ Lipoprotein Particle Concentrations ⦸Lipoprotein particle size |
Mattioli et al. (2017) [Italy] [71] | Retrospective, 7d | Asymptomatic for CVD, premenopausal women, 45–54 yo (n = 425) | N | ABI | ↑ABI (normal range) |
Woo et al. (2018) [China] [72] | Cross section | Healthy, ≥65 yo (n = 4000) | N | ABI (ankle brachial index) | ⦸ ABI |
Gardener et al. (2014) [USA] [73] | Cross section | No stroke history, resided in Northern Manhattan, >40 yo (n = 1374) | N | cIMT, Plaque Presence, Plaque Thickness, and Total Plaque Area (TPA) | ⦸ cIMT, ⦸ Plaque Presence, ↓Plaque Thickness, ↓TPA |
Angelis et al. (2020) [Athens, Greece] [74] | Cross section | Clinically stable congestive heart failure (CHF) Males, 18 yo+, left ventricular ejection fraction less than or equal to 40%, symptoms according to New York Heart Association class II or higher, and taking medication (n = 150) | Y | PWV: Pulse Wave Velocity; AIx: Augmentation index; cIMT: Carotid Intima Media Thickness; EF: Ejection Fraction; SRV: Systolic Wave of Tricuspid Annulus; LA: Left atrium; GLPS: global longitudinal strain of the left ventricle, VO2 Max, VE/VCO2, Pulse Pressure | ↓cIMT, AI x ↑SRV ⦸all other variables |
Peñalvo et al. (2016) [Spain] [75] | Cross section | Free of clinical CVD, 40–54 yo (n = 4082) [Progression of Early Subclinical Atherosclerosis] | N | Agatston Score (AG), CAC, Any Plaque Presence, Plaque in Aorta (PA), Carotids (PC), Femorals (PF), & Iliac (PI) | (When compared to Western and Social-Business DP):↓AG, ↓CAC Presence, ↓Any Plaque, ↓PA, PC, PF, & PI |
Uzhova et al. (2018) [Madrid, Spain] [76] | Cross section | Men, 40–55 yo (n = 1798) | N | CACS, Plaque in Femorals (PF) and/or Carotids (PC), and Atherosclerosis | ↓PF, ⦸CACS, ⦸PC, ↓Atherosclerosis |
Frölich et al. (2017) [Germany] [77] | Prospective, 5y | Free of Clinical CHD, 45–75 yo (n = 3718) | Y | CAC | ↓CAC progression & CAC degree |
Whelton et al. (2015) [USA] [78] | Prospective, 9.6y | Free of clinical CVD, Multi-ethnic, 45–84 yo (n = 1850) | N | CAC | ⦸ CAC |
Viskovic et al. (2013) [Zagreb, Croatia] [79] | Cross section | HIV-infected on ART for 12-months or more, and non-HIV infected, adults 18+ yo, no other serious health conditions or medications (n = 241) | N | Subclinical atherosclerosis (defined as CIMT ≥ 0.9 mm and/or the presence of ≥1 carotid plaque) | HIV-Infected: ↓subclinical atherosclerosis (cIMT ≥ 0.9 mm or carotid plaques) |
Akgüllü et al. (2015) [Turkey] [80] | Cross section | CAD Diagnosis, 35–80 yo (n = 200) | N | GS (Gensini Score) | ↓GS |
Gomez Sanchez et al. (2020) [Spain] [81] | Cross section | 35–75 yo, without CVD or any other chronic conditions (n = 500) | Y | early vascular aging (vascular damage in carotid arteries or peripheral artery disease were classified as EVA and subjects at the percentile of the combined Vascular Aging Index (VAI) were classified; ≥p90 was considered EVA and <p90 was considered normal vascular aging (NVA)), carotid-femoral pulse wave velocity (cfPWV), and cIMT | ↑MedDiet: ↓EVA ↑NVA |
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Richardson, L.A.; Izuora, K.; Basu, A. Mediterranean Diet and Its Association with Cardiovascular Disease Risk Factors: A Scoping Review. Int. J. Environ. Res. Public Health 2022, 19, 12762. https://doi.org/10.3390/ijerph191912762
Richardson LA, Izuora K, Basu A. Mediterranean Diet and Its Association with Cardiovascular Disease Risk Factors: A Scoping Review. International Journal of Environmental Research and Public Health. 2022; 19(19):12762. https://doi.org/10.3390/ijerph191912762
Chicago/Turabian StyleRichardson, Leigh Ann, Kenneth Izuora, and Arpita Basu. 2022. "Mediterranean Diet and Its Association with Cardiovascular Disease Risk Factors: A Scoping Review" International Journal of Environmental Research and Public Health 19, no. 19: 12762. https://doi.org/10.3390/ijerph191912762